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A decrease in hepatitis C virus RNA to undetectable levels in chronic hepatitis C patients after PegIFNα + RVB or

Allison Cázares-Cortazar1, Luis A Uribe-Noguez1, José Antonio Mata-Marín2

  • 1Laboratorio Central de Epidemiología, División de Laboratorios de Vigilancia e Investigación Epidemiológica, Instituto Mexicano del Seguro Social, IMSS, Calzada vallejo s/n Col. La Raza, Del. Azcapotzalco, CP 02990, México City, México.

Archives of Virology
|September 5, 2020
PubMed

Insights

Hepatitis C virus (HCV) infection causes oxidative stress and insulin resistance. Antiviral treatments reduced insulin resistance, but oxidative stress markers persisted, suggesting insulin resistance is a biomarker for direct-acting antiviral therapy effectiveness.

Area of Science:

  • Hepatology
  • Virology
  • Metabolic Syndrome

Background:

  • Hepatitis C virus (HCV) infection is linked to oxidative stress (OS) and insulin resistance (IR), contributing to chronic hepatitis C (CHC) complications and hepatocellular carcinoma.
  • Investigating the impact of antiviral therapies on OS and IR is crucial for managing CHC progression.

Purpose of the Study:

  • To evaluate the effects of pegylated interferon alpha + ribavirin (PegIFNα+RVB) and sofosbuvir + NS5A inhibitor (SOF+InNS5A) on insulin resistance and oxidative stress markers in CHC patients.
  • To determine if insulin resistance can serve as a biomarker for treatment response to direct-acting antivirals.

Main Methods:

  • HCV genotyping was performed on 20 CHC patients, divided into two treatment groups: PegIFNα+RVB (n=10) and SOF+InNS5A (n=10).
  • Assessed OS markers (lipid and protein damage, DNA damage, inflammatory cytokines, GSH), liver enzymes (ALT, AST), platelet count, and insulin resistance (HOMA1-IR index).
  • Measured superoxide dismutase (SOD) and catalase activity before and after treatment until viral RNA became undetectable.

Main Results:

  • Both treatments led to undetectable viral RNA by week 12 (100% for SOF+InNS5A, 70% for PegIFNα+RVB).
  • Post-treatment, significant increases in platelet count and SOD activity were observed, alongside decreases in ALT, insulin, and IR (p<0.05), irrespective of treatment or genotype.
  • The SOF+InNS5A group showed increased oxidative damage to lipids and proteins (p<0.05), while OS markers generally persisted post-treatment.

Conclusions:

  • Antiviral therapy effectively reduces insulin resistance in CHC patients, with IR potentially acting as a response biomarker for direct-acting antivirals.
  • Oxidative stress markers persist even after successful viral clearance, indicating ongoing cellular damage.
  • The SOF+InNS5A regimen demonstrated a more pronounced impact on specific oxidative damage markers compared to PegIFNα+RVB.

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